Reduced 11 beta-hydroxysteroid dehydrogenase activity in patients with thenephrotic syndrome

Citation
B. Vogt et al., Reduced 11 beta-hydroxysteroid dehydrogenase activity in patients with thenephrotic syndrome, J CLIN END, 84(2), 1999, pp. 811-814
Citations number
27
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
ISSN journal
0021972X → ACNP
Volume
84
Issue
2
Year of publication
1999
Pages
811 - 814
Database
ISI
SICI code
0021-972X(199902)84:2<811:R1BDAI>2.0.ZU;2-R
Abstract
Patients with the nephrotic syndrome (NS) exhibit abnormal renal sodium ret ention which cannot completely explained by a secondary hyperaldosteronism due to reduced renal perfusion. As an alternative mechanism to explain this phenomenon we postulate a cortisol-mediated mineralocorticoid effect as a consequence of a reduced activity of 11 beta-hydroxysteroid dehydrogenase ( 11 beta-HSD). A down-regulation of 11 beta-HSD, i.e. of the shuttle of acti ve to inactive glucocorticosteroids, has been shown to cause mineralocortic oid effects. Therefore we investigated the activity of 11 beta-HSD by measu ring the urinary ratio of (tetrahydrocortisol + 5 alpha-tetrahydrocortisol) /tetrahydrocortis [(THF+5 alpha-THF)/THE] by gas-chromatography in 29 NS pa tients with biopsy-proven glomerulonephritis and 29 healthy control subject s. The ratio of (THF+5 alpha-THF)/THE was higher in NS patients (median 1.4 9, range 0.45-4.07) than in the control subjects (0.98, 0.60-1.36; p<0.01). This ratio was increased as a consequence of a decreased urinary excretion rate of the cortisone metabolite, THE. The present data indicate that a re duced activity of 11 beta-HSD is a new mechanism contributing to the exagge rated sodium retention in patients with the NS.